ArticleFrontiers in immunology2021
Innate Immune Cytokine Profiling and Biomarker Identification for Outcome in Dengue Patients.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Profiling an Enhanced IL-6 Expression Distinguishes Host Susceptibility to Primary and Secondary Infections of the Dengue Virus in an Ex Vivo Whole-Blood Coculture Model.Journal of tropical medicine · 2026Article
- Elevated Interleukin-37 Associated with Dengue Viral Load in Patients with Dengue Fever.Current microbiology · 2023Article
- Who Knew? Dopamine Transporter Activity Is Critical in Innate and Adaptive Immune Responses.Cells · 2023Article
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Early biomarkers of progression to severe dengue are urgently required to enable effective patient management and control treatment costs. Innate immune cells, which comprise the earliest responders to infection and along with the cytokines and chemokines they secrete, play a vital role in orchestrating the subsequent adaptive immune response and have been implicated in the enhancement of infection and "cytokine storm" associated with dengue severity. We investigated the early innate immune cytokine profile of dengue patients during acute phase of disease in a prospective blinded study that included subjects with acute dengue and febrile controls from four major hospitals in Bengaluru, India along with healthy controls. We used intracellular cytokine staining and flow cytometry to identify innate immune biomarkers that can predict progression to severe dengue. Results: Dengue infection resulted in enhanced secretion of multiple cytokines by all queried innate immune cell subsets, dominated by TNF-α from CD56 Conclusion: Our findings suggested that faulty/delayed kinetics of innate immune activation and downregulation was a driver of disease severity. We identified IFN-
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